ArticleCell death & disease2022
Mice with Trp53 and Rb1 deficiency in chondrocytes spontaneously develop chondrosarcoma via overactivation of YAP signaling.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- Dedifferentiated Chondrosarcoma: Current Advances and Future Perspectives.Current treatment options in oncology · 2026Review
- Proton Irradiation Induces Differential Cellular Responses and Proteomic Signatures in Chondrosarcoma and Chondrocytes.Current issues in molecular biology · 2026Article
- Engineering Osteosarcoma In Vitro: From Traditional Models to Biofabricated Platforms for Precision Medicine.ACS omega · 2025Review
- Chondrosarcoma: New Molecular Insights, Challenges in Near-Patient Preclinical Modeling, and Therapeutic Approaches.International journal of molecular sciences · 2025Review
- KDELR1 regulates chondrosarcoma drug resistance and malignant behavior through Intergrin-Hippo-YAP1 axis.Cell death & disease · 2024Article
- Emerging role and function of Hippo-YAP/TAZ signaling pathway in musculoskeletal disorders.Stem cell research & therapy · 2024Review
- IFT20 and WWTR1 govern bone homeostasis via synchronously regulating the expression and stability of TβRII in osteoblast lineage cells.Research square · 2024Article
- Dedifferentiated Chondrosarcoma from Molecular Pathology to Current Treatment and Clinical Trials.Cancers · 2023Review
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Chondrosarcoma (CHS) is a rare type of soft sarcoma with increased production of cartilage matrix arising from soft bone tissues. Currently, surgical resection is the primary clinical treatment for chondrosarcoma due to the poor response to radiotherapy and chemotherapy. However, the therapeutic effect is not satisfactory due to the higher local recurrence rate. Thus, management and elucidation of the pathological mechanism of chondrosarcoma remain an ongoing challenge, and the development of effective chondrosarcoma mouse models and treatment options are urgently needed. Here, we generated a new transgenic chondrosarcoma model by double conditional deletions of Trp53 and Rb1 in chondrocyte lineage which spontaneously caused spinal chondrosarcoma and lung metastasis. Bioinformatic analysis of the human soft sarcoma database showed that Trp53 and Rb1 genes had higher mutations, reaching up to approximately 33.5% and 8.7%, respectively. Additionally, Trp53 and Rb1 signatures were decreased in the human and mouse chondrosarcoma tissues. Mechanistically, we found that YAP expression and activity were significantly increased in mouse Col2-Cre;Trp53
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